In Friedreich’s ataxia, expansions of unstable nucleotide repeats in the FXN gene result in reduced expression of frataxin (Campuzano et al., 1996), a protein thought to act as molecular chaperone in iron-sulfur clusters and heme biosynthesis as well as iron storage site (Alsina et al., 2018). Here, FXN is linked to Friedreich ataxia.